Autoimmune diseases hold significant importance in the realm of medical research, prompting a thorough exploration of potential therapeutic interventions. One crucial aspect of this exploration involves understanding the intricate processes of histone acetylation and deacetylation. Histone acetylation, facilitated by histone acetyl transferases (HATs), is instrumental in rendering DNA transcriptionally active.
View Article and Find Full Text PDFBackground: Aberrant expression of histone deacetylases (HDACs) and ribonucleotide reductase (RR) enzymes are commonly observed in various cancers. Researchers are focusing on these enzymes in cancer studies with the aim of developing effective chemotherapeutic drugs for cancer treatment. Targeting both HDAC and RR simultaneously with a dual HDAC/RR inhibitor has exhibited enhanced effectiveness compared to monotherapy in cancer treatment, making it a promising strategy.
View Article and Find Full Text PDFThe development of cancer is influenced by several variables, including altered protein expression, and signaling pathways. Cancers are inherently heterogeneous and exhibit genetic and epigenetic aberrations; therefore, developing therapies that act on numerous biological targets is encouraged. To achieve this, two approaches are employed: combination therapy and dual/multiple targeting chemotherapeutics.
View Article and Find Full Text PDFHistiocytosis represents a group of uncommon disorders characterized by the abnormal accumulation of specialized immune cells, such as macrophages, dendritic cells, or monocyte-derived cells, in various tissues and organs. Over 100 distinct subtypes have been documented, each displaying a broad spectrum of clinical presentations and histological characteristics. Till today, histiocytosis has been addressed through a combination of chemotherapy, radiotherapy, and surgery, with varying responses from individual patients.
View Article and Find Full Text PDFHistone deacetylase 2 (HDAC 2) of class I HDACs plays a major role in embryonic and neural developments. However, HDAC 2 overexpression triggers cell proliferation by diverse mechanisms in cancer. Over the decades, many pan and class-specific inhibitors of HDAC were discovered.
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